ArticleHepatic medicine : evidence and research2011
Inhibition of Notch signaling affects hepatic oval cell response in rat model of 2AAF-PH.
Article in Hepatic medicine : evidence and research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 26 citations in OpenAlex.
- Notch Inhibition Promotes Differentiation of Liver Progenitor Cells into Hepatocytes viaStem cells international · 2019Article
- The diversity and plasticity of adult hepatic progenitor cells and their niche.Liver international : official journal of the International Association for the Study of the Liver · 2017Review
- Hepatic progenitor cell activation in liver repair.Liver research (Beijing, China) · 2017Article
- Vascular patterning sets the stage for macro and micro hepatic architecture.Developmental dynamics : an official publication of the American Association of Anatomists · 2015Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND AND
aimsActivation of the oval cell compartment occurs in the liver when hepatocytes are functionally compromised and/or unable to divide. Our goal was to investigate the systemic signals responsible for determining the efficiency of oval cell-mediated liver regeneration, focusing on the Notch signaling cascade.
methodsThe established oval cell induction protocol of 2-acetylaminofluorine (2-AAF) implantation followed by 70% surgical resection of the liver (partial hepatectomy, PH) was employed in a rat model. This oval cell induction model was further combined with injections of a γ-secretase inhibitor (GSI XX) to examine the effects of Notch inhibition on oval cell-aided regeneration of the liver.
resultsNotch signaling was found to be upregulated at the peak of oval cell induction during 2AAF-PH alone. Treatment with GSI XX led to interruption of the Notch signal, as shown by a decrease in expression of Hes1. While there was a robust oval cell response seen at day 11 post-PH, there was a measurable delay in differentiation when Notch was inhibited. This was confirmed morphologically as well as by immunohistochemistry for the oval cell markers, α-fetoprotein, OV-6, and CK19. The hepatocytes seen at day 22 demonstrated an enhanced hepatocellular mitoinhibition index (p21(Waf1)/Ki67), suggestive of dysregulated proliferation and cell cycle progression. Moreover, these hepatocytes exhibited decreased expression of hepatocyte functional markers, such as cytochrome P450 and glucose-6-phosphatase-α.
conclusionsTaken together, these results identify the Notch signaling pathway as a potent regulator of differentiation and proliferation in oval cells, which is necessary for functional for repair of the liver by oval cells.
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